Tissue factor-induced Thrombin Generation in the Fasting and Postprandial State among Elderly Survivors of Myocardial Infarction

Introduction

Tissue factor (TF)-induced thrombin generation (TG) ex vivo has been suggested to be an important method to assess thrombotic risk. No studies have investigated the impact of postprandial lipemia on TF-induced TG. Since myocardial infarction (MI) is associated with elevated postprandial levels of triglycerides, we hypothesized a differential impact of postprandial lipemia on coagulation activation in MI-patients and healthy controls.

Material and Methods

Elderly survivors of acute MI (n = 44) and healthy age-and sex matched controls (n = 43) underwent a fat tolerance test (1 gram per kg body weight) to assess coagulation activation during postprandial lipemia.

Results

The incremental area under the curve (AUCi) for serum triglycerides was higher in MI-patients than in healthy age-and sex matched controls (5.64 ± 0.52 mmol/L?h and 3.94 ± 0.39 mmol/L?h, p = 0.012) during the postprandial phase. Subsequent endogenous activation of coagulation, assessed by FVIIa and thrombin generation (F1 + 2), was similar among groups and not related to levels of triglycerides during the postprandial phase. Healthy individuals had a gradual decline in TF-induced thrombin generation ex vivo, assessed by endogenous thrombin potential (ETP) (AUCi = - 542.4 ± 71.4 nM?min?h, p < 0.001), whereas MI-patients retained their ETP (AUCi = 127.4 ± 89.0 nM?min?h, p = 0.47) in plasma during the postprandial phase (p for group difference = 0.005).

Conclusions

MI-patients had elevated postprandial lipemia and retained their ability for TF-induced TG in plasma ex vivo in the postprandial phase, whereas the capacity gradually decreased in healthy individuals. Further studies are warranted to reveal underlying mechanism(s) and clinical implications.     

Endothelial function and postprandial lipemia

It is widely recognised that post-prandial lipoproteins play a role in the development of atherosclerosis, but the mechanisms underlying this role are unclear. An attractive working hypothesis is that the pathogenetic link is endothelial dysfunction. The available data seem to corroborate this theory and recognise triggering by oxidative stress, but some of the evidence is still contradictory.     

Evaluation of Dietary Intake,Leisure-Time Physical Activity,and Metabolic Profile in Women with Mutation in the LMNA Gene

Introduction: Familial partial lipodystrophy (FPL) is a rare genetic disorder characterized by selective lack of subcutaneous fat, which is associated with insulin-resistant diabetes. The Dunnigan variety (FPLD2) is caused by several missense mutations in the lamin A/C (LMNA) gene, most of which are typically located in exon 8 at the codon position 482.

Objective: The aim of this study was to assess and compare the dietary intake, leisure-time physical activity (LTPA), and biochemical measurements (glucose, A1C, and plasma lipids) in women with FPLD2 and without (control group, CG) and to examine the associations between dietary intake and biochemical measurements (BM).

Methods: LTPA was measured with a questionnaire and metabolic equivalent (MET) hours per week (hours/week) were calculated. Dietary intake by the 3-day recall method and clinical laboratory parameters were collected.

Results: Characteristics of women with FPLD2: 35.8 ± 13.9 years, fat mass = 10 ± 2.3 kg and fat free mass = 41.4 ± 4.5 kg (p < 0.05). Women with FPLD2 showed a smaller intake of energy (kcal), lipids, and carbohydrates and a large intake of protein (p < 0.01) compared to CG. Comparing the 2 groups in terms of LTPA, 78% of women with FPLD2 performed insufficient physical activity. In addition, they had a higher levels of glucose, A1C, and triglycerides (TG) and lower levels of high-density lipoprotein (HDL). There was no correlation between dietary intake and biochemical measurements.

Conclusions: Women with FPLD2 have a lower intake of energy (kcal), lipids, and carbohydrates and greater changes in biochemical measurements. Because this is a rare disease, future studies are needed with encouragement of the practice of physical activity and of healthy eating habits, preventing the onset of diseases.     

某高校老年高血压患者体重指数与血脂、脂肪肝的相关性探讨

目的探讨老年高血压患者体重指数与脂肪肝、血脂及血压之间的关系。方法对参加校体检所有人员均进行病史询问并检查血压、体重、身高、腰围、臀围、心电图、胸透、眼底检查、空腹12小时的晨生化检查、尿常规检查、空腹上腹部B超检查。对资料完整离退休高血压患者313例,按体重指数(BMI)分为三组:正常体重组,超重组,肥胖组,进行分析。结果肥胖组、超重组TC、TG、LDL均高于正常组,有显著性差异(P<0.05),BMI与脂肪肝的发生率呈正相关(rs=0.911,P<0.01),肥胖组与正常组、超重组比较收缩压及舒张压均明显升高,超重组较正常组血压值高。结论肥胖高血压患者应减轻体重,BMI应控制在正常范围,对控制高血压、高脂血症、冠心病、糖尿病、脂肪肝的发生发展,降低心脑血管事件的发生有重要的意义。     

不同程度的脂血和黄疸对酶法测定血清钾干扰的分析

目的:探讨不同程度的脂血及黄疸对酶法测定血清钾结果的影响.方法:对不同程度的脂血及黄疸标本的血清钾分别采用酶法及离子选择电极(ISE)法进行检测.结果:当血清甘油三酯(TG)水平＞10.0 mmol/L时,有部分标本不能用酶法测定,而当血清TG水平＞15.0 mmol/L时,大部分标本不能用酶法测定.酶法与ISE法的相关性良好(r=0.926 6),但测定结果有明显差异(P＜0.01).而黄疸对酶法测定血清钾无明显干扰,两法的相关性良好(r=0.990 3),测定结果也有明显差异(P＜0.01).结论:黄疽及中度脂血(TG＜10.0 mmol/L)对酶法测定血清钾无明显干扰,但酶法不适用于严重脂血标本(TG＞10.0 mmol/L).     

Effects of hemolysis and lipemia interference on kaolin-activated thromboelastography,and comparison with conventional coagulation tests

The effects of hemolysis and lipemia on thromboelastography (TEG) analysis have been scarcely evaluated in human samples, and neglected in clinical practice. We aimed to investigate the effects of in vitro mechanical hemolysis and lipemia on TEG analysis and conventional coagulation tests. Twenty-four healthy volunteers were enrolled in the study. Besides the controls, three groups with slight, moderate and severe mechanical hemolysis were constituted according to free hemoglobin (Hb) concentrations of 0.5–1.0, 2.0–6.0 and 7.0–13.0?g/L, respectively; and three groups with mild, moderate and high lipemia were established according to triglyceride concentrations of ～6.0, ～12.0, and ～18.0?mmol/L, respectively. Four TEG parameters, reaction time (R), coagulation time (K), angle (α), and maximum amplitude (MA), were measured alongside conventional plasma tests including prothrombin time (PT), activated partial thromboplastin time (APTT) and fibrinogen (FIB) by mechanical method, and platelet count by optical method. Results showed that the median R and MA values at moderate and severe hemolysis and K at severe hemolysis exceeded respective reference intervals, and were considered unacceptable. Median values of TEG parameters in lipemic samples were all within reference intervals. Bias values of conventional plasma tests PT, APTT and FIB in hemolyzed or lipemic samples were all lower than the Clinical Laboratory Improvement Amendments (CLIA) allowable limits. Bias values of platelet count at moderate to severe hemolysis and lipemia exceeded the CLIA allowable limits. In conclusion, the detection of TEG was in general more affected by mechanical hemolysis than plasma coagulation tests. Pre-analytical variables should be taken into account when unexpected TEG results are obtained.     

Effects of fenofibrate on endothelial function and cell adhesion molecules during post-prandial lipemia in hypertriglyceridemia

BACKGROUND: Fasting and post-prandial hypertriglyceridemia have been associated with endothelial dysfunction. OBJECTIVE: To investigate the effects of a 3-month treatment with fenofibrate (200 mg daily) on endothelial reactivity and inflammatory state in hypertriglyceridemic patients at fast and after an oral fat load. METHODS: Brachial flow-mediated vasodilation (FMV) and the circulating levels of intercellular adhesion molecule (ICAM) and vascular cellular adhesion molecule (VCAM) were determined in 10 hypertriglyceridemic patients. RESULTS: Before treatment, post-prandial phase was characterized by an increase in triglycerides (3.7 +/- 1 mmol/L at baseline vs. 4.2 +/- 1, 6.5 +/- 1, 6.6 +/- 2, and 5.3 +/- 2 mmol/L after 2, 4, 6, and 8 h), a decrease in FMV (4.3 +/- 2% at baseline vs. 2.8 +/- 1, 2.2 +/- 1, and 1.3 +/- 1% after 2, 4, and 6 h), and an increase in ICAM and VCAM. After fenofibrate there was a significant reduction in fasting triglycerides (3.7 +/- 1.3 vs. 2.1 +/- 0.8 mmol/L), ICAM (480 +/- 113 vs. 269 +/- 65 ng/mL) and VCAM (1821 +/- 570 vs. 1104 +/- 376 ng/mL), and an increase in FMV (4.3 +/- 2 vs. 7.1 +/- 2%). Post-prandially triglycerides increased (2.1 +/- 1 at baseline vs. 2.4 +/- 2 and 3.6 +/- 1 mmol/L after 4 and 6 h), FMV decreased (7.1 +/- 2 at baseline vs. 5.8 +/- 2, 5.5 +/- 2, 5.9 +/- 2, 6.4 +/- 2% after 2, 4, 6, and 8 h), and there was an increase of ICAM and VCAM. Before therapy post-prandial changes in FMV had an inverse correlation with the changes in triglycerides (r = -0.34; P < 0.05) and ICAM (r = -0.66; P < 0.001). CONCLUSIONS: The transient endothelial dysfunction observed in hypertriglyceridemic subjects during post-prandial lipemia is mediated by post-prandial triglyceride increase and by the activation of inflammatory response. The anti-inflammatory activity of fenofibrate may represent an additional mechanism of its favorable action on the endothelial function during fasting and the post-prandial phase.     

Association between postprandial triglycerides and coronary artery disease detected by coronary computed tomography angiography

Background

Studies have demonstrated the association of severe anatomical coronary artery disease (CAD) with postprandial triglycerides (TG) concentrations. Nevertheless the relationship between less severe atherosclerosis plaque burden and postprandial TG is less established.

Objective

to study the relationship between postprandial TG and CAD detected by coronary computed tomographic angiography (CTA).

Material and methods

130 patients who underwent an oral fat tolerance test were enrolled (85 with CAD detected by CTA and 45 without). Postprandial lipemia was studied by measuring TG from T0h to T6h with 2-h intervals, and analyzed the TG change over time using a longitudinal multivariable linear mixed effects model with the log normal of the TG as the primary outcome.

Results

The majority of individuals with CAD had non-obstructive disease (63.3%) Patients with CAD had a slower clearance of postprandial TG change from 4 h to 6 h (p < 0.05) compared to patients without CAD. These results remained significant after adjustment for fasting TG and glucose, age, gender, body mass index, and waist circumference. However, those differences did not reach statistical significance after adjustment for fasting HDL-C.

Conclusion

Patients with mild (<25% lumen obstruction) and moderate CAD (25–50% lumen obstruction) detected by coronary CTA had an impaired postprandial metabolism, with a delayed TG clearance, when compared to individuals with no CAD. This difference was partially explained by the lower HDL-C. Thus, though postprandial TG may contribute to the development of CAD, this association is partially related to low HDL-C.     

Resistance exercise at variable volume does not reduce postprandial lipemia in postmenopausal women

GeroScience - The aim of this study was to investigate the acute effects of resistance exercise sessions (RESs) performed at different levels of high-volume resistance exercise (HVRE) and...     

Diurnal Triglyceridemia in Relation to Alcohol Intake in Men

Fasting and postprandial triglyceride concentrations largely depend on dietary and lifestyle factors. Alcohol intake is associated with triglycerides, but the effect of alcohol on diurnal triglyceridemia in a free living situation is unknown. During three days, 139 men (range: 18–80 years) measured their own capillary triglyceride (cTG) concentrations daily on six fixed time-points before and after meals, and the total daily alcohol intake was recorded. The impact of daily alcohol intake (none; low, <10 g/day; moderate, 10–30 g/day; high, >30 g/day) on diurnal triglyceridemia was analyzed by the incremental area under the cTG curve (∆cTG-AUC) reflecting the mean of the six different time-points. Fasting cTG were similar between the alcohol groups, but a trend of increased cTG was observed in men with moderate and high alcohol intake after dinner and at bedtime (p for trend <0.001) which persisted after adjustment for age, smoking and body mass index. The ∆cTG-AUC was significantly lower in males with low alcohol intake (3.0 ± 1.9 mmol·h/L) (n = 27) compared to males with no (7.0 ± 1.8 mmol·h/L) (n = 34), moderate (6.5 ± 1.8 mmol·h/L) (n = 54) or high alcohol intake (7.2 ± 2.2 mmol·h/L) (n = 24), when adjusted for age, smoking and body mass index (adjusted p value < 0.05). In males, low alcohol intake was associated with decreased diurnal triglyceridemia, whereas moderate and high alcohol intake was associated with increased triglycerides after dinner and at bed time.